Q: What drug inhibits proteolysis (release of T3/T4 from thyroglobulin) via Wolff Chaikoff Effect? A: Potassium Iodide. When you intake a lot of Iodide, you get negative feedback and inhibit T3/T4 release.

Q: What drug can you use to decrease the size and vascularity of the thyroid gland in preparation of surgery? A: Thioamies, Potassium Iodide.

Q: What drug do you use to prevent thyroid from absorbing radioactive iodide, like from radioactive poisoning? A: Potassium Iodide, because it saturates the thyroid so other types of iodide can’t get in.

Q: What drug can cause fetal goiter when used during pregnancy? A: Potassium Iodide.

Q: What drug do you take as an alternative to surgery for Thyroid cancer? A: Radioactive Iodide 131. You also take it to get rid of any microscopic traces of the cancer after surgery.

Q: What drug can destroy the fetus thyroid if you take it during pregnancy? A: Radioactive Iodide 131, because it can cross the placenta because it is lipid soluble. So you can take it per os as well.

Q: What happens after you take Radioactive Iodide 131? A: You become permanently hypothyroid, since you don’t have a thyroid anymore. You need to take Hormone Replacement Therapy for the rest of your life, which is easier to deal with than hyperthyroidism.

Q: How long does it take Radioactive Iodide 131 to destroy the thyroid? A: 1-3 months

Q: What class of drugs competitively block iodine uptake into follicular cells in thyroid glands? A: Anion Inhibitors (the anion is the iodide)

Q: What is the drug of choice for Myxedema Coma? A: Levothyroxine (T4) – because it converts to the active T3 when needed. It’s cheap,stable (since it’s inactive), and has a loooong halflife (vs. active T3).

Q: What Myxedema Coma drug can give you cardiotoxicity like MI, Arrhythmia, and Angina and therefore contraindicated in cardiac patients? A: Liothyronine (T3)

Q: When would you use T3? A: Only during EMERGENCIES, in extreme cases of myxedema coma when you need to replenish T3 quickly. T4 you have to wait for it to convert to T3.

Q: What’s the mortality rate for Myxedema Coma? A: 50%. It’s not really a coma, but you can get unconscious. It is basically extreme hypothyroidism.

Q: How do you prevent adrenal crisis (severe adrenal insufficiency due to the decrease in the number of adrenal steroid receptors you have)? A: By tapering off the dosage of the drug, instead of suddenly withdrawing it.

Q: What does POMC break down into? A: ACTH, gamma-MSH, and beta-Lipotropin.

Q: What are the layers of the Adrenal cortex and what do they produce? A: ATII, K+ stimulate Zona Glomerulosa to produce Aldosterone (Mineralocorticoids) – because only zona glomerulosa have 18-hydroxylase ACTH stimulate Zona Fasciculata to produce Cortisol (Glucocorticoids) ACTH stimulate Zona Reticularis to produce Androgens

Q: What ACTH analogue is used to diagnose CAH and Adrenal Insufficiency (Addison’s)? A: Cosyntropin. It stimulates Cholesterol Desmolase (Cytochrome P450 SCC), increasing 17-OH-Progesterone if you have CAH.

Q: What time of day is Cortisol the highest? A: In the morning. Lowest at night when sleeping, just like the Sympathetic Nervous System. So you give doses in the mornings to simulate natural schedule.

Q: If you have increased CRH, increased ACTH, and increased Cortisol, you know the tumor is where? A: Hypothalamus –> secrete too much CRH.

Q: If you have decreased CRH, increased ACTH, and increased Cortisol, you know the tumor is where? A: Pituitary –> secrete too much ACTH.

Q: If you have decreased CRH, decreased ACTH, and increased Cortisol, you know the tumor is where? A: Adrenal Gland –> secrete too much Cortisol.

Q: If you have increased CRH, increased ACTH, and decreased Cortisol, where is the impairment? A: Adrenal Gland –> can’t secrete Cortisol — Addison Disease, CAH –> more ACTH made to “compensate” for the decreased Cortisol –> ACTH breaks down to alpha-MSA –> increased skin pigmentation.

Q: If you have decreased CRH, decreased ACTH, and decreased Cortisol, where is the impairment? A: Hypothalamus or Pituitary — Sheehan Syndrome (Hypopituitary during pregnancy)

Q: Which glucocorticoid has some mineralocorticoid activity and therefore may cause some edema? A: Prednisone

Q: Which glucocorticoids are long-acting and most active? A: Betamethasone and Dexamethasone.

Q: Which glucocorticoids are used to mature fetal lungs? A: Betamethasone and Dexamethasone, because they can penetrate the fetus.

Q: What does a Low-Dose Dexamethasone Suppression Test test for? A: Tests for Cushing’s Disease, Adrenal Tumor, Ectopic Secretions. If you give Dexamethasone (a long-acting glucocorticoid), and there is no negative feedback, then you know something in your body is secreting all that extra cortisol.

Q: Once you establish you got either Cushing’s Disease, Adrenal Tumor, or Ectopic Secretion, what does doing a High-Dose Dexamethasone Suppression Test test for? A: If giving a high dose Dexamethasone suppresses your cortisol levels to normal levels, then you most likely have Cushing’s Disease. If there is no suppression, then measure the basal ACTH. If ACTH level stays the same, then you got ectopic ACTH Tumor. If you have decreased ACTH then you most likely have an adrenal tumor (because of negative feedback).

Q: What inhaled Glucocorticoids are used to treat Asthma because it is restricted to the bronchioles (since it is inhaled)? A: Beclomethasone, Budesonide, Flunisolide, Fluticasone.

Q: What are the adverse effects of Glucocorticoid drugs if you use over 2 weeks? A: Adrenal Suppression. You can also get Cushingoid Syndrome and Osteoporosis.

Q: What drug should you NOT use if you have Hypertension, Peptic Ulcer, Infections, and Diabetes? A: Glucocorticoids. Because remember, Glucocorticoids increase gastric acid, decrease immunity, and DECREASE SENSITIVITY TO INSULIN (and increases glucose in blood).

Q: What drugs do you use to treat Cushing Syndrome (before the main treatment of surgery, of course)? A: Adrenal Steroid Synthesis Inhibitors — Aminoglutethimide, Ketoconazole, Metyrapone, and Mitotane.

Q: Which drug blocks desmolase (blocking the conversion of cholesterol –> pregnenolone) and aromatase (blocking androgen –> Estrogen)? A: Aminoglutethimide… therefore it can be used to treat both Cushing’s Syndrome and Breast Cancer.

Q: Which drug blocks desmolase and 17-20 lyases? A: Ketoconazole

Q: Which drug inhibits adrenal steroid synthesis at low doses but both adrenal and gonadal synthesis at high doses? A: Ketoconazole

Q: Which drug blocks 11-beta hydroxylation, which is the final step in cortisol synthesis? A: Metyrapone. Because it blocks this enzyme, 11-Deoxycortisol accumulates, which has mineralocorticoid action –> AE: water and sodium retention

Q: What drug destroys the adrenal cortex, and therefore can be used to treat adrenal carcinoma? A: Mitotane — not used anymore because it can destroy the adrenal cortex, and carcinomas can be surgically removed.

Q: Which drug blocks progesterone receptors and blocks glucocorticoids at high dose and therefore used to treat adrenal carcinoma? A: Mifepristone

Q: Which drug blocks both aldosterone and androgen? A: Spironolactone

Q: Which drug treats Primary Hyperaldosteronism (hypersecretion of cortisol from adrenal gland) as well as Hirsutism? A: Spironolactone — used for both of these because blocks both aldosterone and androgen.

Q: Which drug is an aldosterone antagonist only? A: Eplerenone — used as adjunct for chronic heart failure.

Q: What are the adverse effects of Estrogen? A: Gall stones, Pulmonary Embolism, and Endometrial/Breast Cancer

Q: What are the three SERMs? A: Clomiphene, Tamoxifen, Raloxifene

Q: Which SERM inhibits the estrogen receptors in the hypothalamus and pituitary rather than in the gonads and therefore inhibit negative feedback by estrogen on FSH/LH production (increasing FSH/LH), and therefore used to treat Infertility? A: Clomiphene

Q: Which SERM gives you multiple pregnancies as an adverse effect? A: Clomiphene

Q: Which SERM is an agonist in bone and lipid, antagonist in breast, and partial agonist in endometrium? A: Tamoxifen. Because it is a partial agonist in endometrium, it has risk of endometrial cancer.

Q: Which SERM is an agonist in bone and lipid, antagonist in breast AND endometrium, and therefore has no risk of endometrial cancer? A: Raloxifene.

Q: Which drug can you use to treat breast cancer? A: Tamoxifen and Raloxifene

Q: Which SERM can be used to treat both breast cancer and osteoporosis in post-menopausal women? A: Raloxifene

Q: What drug is a progesterone receptor partial agonist and a glucocorticoid receptor antagonist (at high dose)? A: Mifepristone — used to terminate pregnancy within 49 days after intercourse, and treats Cushing Syndrome and Adrenal Carcinoma!!

Q: What drug do you take to induce abortion (when egg already implanted) 49 days after intercourse? A: Mifepristone, which is an anti-progestin drug. Unlike progestin, which is used to prevent pregnancy before implantation of egg, mifepriston is an ANTI-progestin, which would induce menstruation, getting rid of any eggs after they are implanted.

Q: What are the first generation Progestins? A: Norethindrone, Ethynodiol diacetate

Q: What are the second generation Progestins? A: Levonorgestrel, Norgestrel

Q: What are the third generation Progestins? A: Desogestrel, Norgestimate

Q: Which androgen receptor antagonist is non-steroidal and therefore does NOT suppress gonadotropin and therefore can treat prostate cancer without the unwanted side effects of decreased testosterone? A: Bicalutamide, Flutamide

Q: What drugs are GnRH agonists used to treat prostate cancer via the negative feedback effect it has on decreasing testosterone levels? A: Goserelin, Buserelin — initially there is an increase in FSH and LH levels due to the “flare effect” but eventually downregulated.

Q: Which drug inhibits 5-alpha-reductase II and therefore used to treat Benign Prostate Hypertrophy, but gives you the adverse effects of erectile dysfunction and gynecomastia? A: Finasteride

Q: What do you get if you are a woman and you have increased LH or insulin, leading to too much androgen, leading to decreased menstruation and ovulation + hirsutism + infertility? A: Polycystic Ovarian disease

Q: What drugs can you use to treat Polycystic Ovarian Disease by lowering insulin? A: Pioglitazone, Rosiglitazone (both of which are Thiazolidenediones) as well as Metformin (which is a Biguanide)

Q: What drugs can you use to restore fertility in patients with Polycystic Ovarian Disease? A: Clomiphene Citrate or FSH

Q: What drugs can you use to treat the Hirsutism and Acne found in Polycystic Ovarian disease? A: Anti-androgens like spironolactone (which remember is antagonist for androgens as well as aldosterone)

Q: Which drugs can you use to restore menstruation and prevent endometrial hyperplasia in Polycystic Ovarian disease? A: Oral contraceptives

BONE DRUGS

Q: Normal bone density has a T-score of what? A: -1 to +1

Q: Osteopenia has a T-score of what? A: -1 to -2

Q: Osteoporosis has a T-score of what? A: less than -2.5

Q: What increases Calcium and decreases phosphate in the plasma? A: PTH

Q: PTH works mainly in what organ and Vitamin D works mainly in what organ? A: PTH works in kidneys. Vitamin D works in intestines.

Q: What drug is a recombinant PTH and makes use of PTH’s property of increasing bone formation at low intermittent doses? A: Teriparatide

Q: What increases calcium and phosphate in plasma but doesnt do it by destroying bone? A: Vitamin D

Q: What class of drugs attach and become part of the bone and can’t be hydrolyzed by osteoclasts because it has Phos-C-Phos rather than the Phos-O-Phos structure of natural bone? A: Bisphosphonates — Alendronate, Risedronate, Ibandronate, Pamidronate, Zoledronate

Q: What drug is used to treat Osteoporosis, Paget’s Disease of Bone, and Hypercalcemia of Malignancy (which is due to proliferation of osteoclasts)? A: Bisphosphonates — because it blocks FPP Synthase, which inhibit osteoclast from attaching to bone. So even if you get a proliferation of osteoclasts, they can’t attach to bone.

Q: What drugs can treat Paget’s Disease of Bone? A: Bisphosphonates and Calcitonin

Q: What class of bone drugs cause Esophagitis and GI Distress, and therefore you tell patient to take lots of water with it and don’t lay down? A: Bisphosphonates

Q: What type of drug inhibits IL-1 and TNF and therefore decrease osteoclast differentiation and activity, and therefore used to prevent osteoporosis in post-menopausal women? A: Estrogen

Q: What SERM is used to prevent osteoporosis in post-menopausal women? A: Raloxifene

Q: What hormone is released from parafollicular cells in thyroid when plasma calcium increases and decreases BOTH calcium and phosphate levels in the plasma? A Calcitonin (“tones” down calcium and phosphate in blood)

Q: What drug is a human monoclonal antibody that inhibits RANKL (found on osteoblasts to activate osteoclast maturation), and therefore osteoclasts can’t mature, and therefore used to treat osteoporosis? A: Denosumab

Q: What are the first and second line of treatments for osteoporosis? A: First line — Bisphosphonates, Raloxifene Second line — Teriperatide, Calcitonin (but only use these if patient can’t use bisphosphonates due to Esophagitis, GI Distress etc.)

Q: What is the anticoagulant of choice for pregnancy? A: Heparin, becuase it is ionized and can’t cross placenta. It can’t be taken orally as well for the same reason.

Q: What drug has risk of thrombocytopenia (along with the usual, like bleeding, osteoporosis)? A: Heparin — known has HIT — heparin-induced thrombocytopenia

Q: What test do you use to monitor heparin levels so you don’t get Heparin-Induced Thrombocytopenia (HIT)? A: aPTT (Active Partial Prothrombin Time, which measures efficacy of intrinsic + common pathway).

Q: Why don’t you give anticoagulants intramuscularly? A: Because your muscles have a lot of vessels and therefore if you puncture through here and prevent clotting, you’ll get a hematoma!!

Q: What do you give to treat Heparin overdose (i.e. person bleeding profusely)? A: Protamine Sulfate, which is a strong base, so it neutralizes heparin, which is a strong acid.

Q: What drug acts just like LMWH’s, inhibiting 10a, but is a different type of molecular (a synthetic pentasaccharide) and has lower risk of HIT than LMWH? A: Fondaparinux

Q: What drugs inhibit thrombin directly and used when patients can’t use heparin (like if they have HIT or something)? A: Direct Thrombin Inhibitors — Hirudin, Argatroban, Lepirudin

Q: What anticoagulant drug is derived from leeches? A: Hirudin — that’s how they suck your blood without clotting!

Q: What drug is similar to LMWH in that it selectively inhibits Factor 10a but is made up of Heparan Sulfate + Dermatan Sulfate + Chondroitin Sulfate (all GAG’s), but it’s not used anymore because it gives you stroke? A: Danaproid

Q: What are the three Vitamin K Antagonists? A: Warfarin, Dicumoral, and Phenindione

Q: Why is there an initial transient clotting risk if you use Vitamin K Antagonist? A: Because Protein C in liver is depleted before the clotting factors. So there’s a short period of time after you take the drugs where you can’t prevent clots and you still have the clotting factors. Therefore you treat concurrently with heparin initially for 3-5 days to prevent these risks.

Q: What anti-platelet drug causes neutropenia and thrombocytopenia and therefore not used anymore? A: Ticlopidine

Q: What is the best anti-platelet drugs for people who can’t take aspirin (because they have GI bleeding or peptic ulcers)? A: Clopidogrel

Q: What anti-platelet drug blocks COX, and therefore prevents synthesis of TXA2 (thromboxane, which CAUSES clotting) but also PGI2 (prostacyclin, which PREVENTS clotting) at high doses? A: Aspirin. Give at low doses to spare the PGI2 needed to prevent clotting.

Q: What are the five main types of hyperlipoproteinemia drugs? A: Resins, Statins, Fibrates, Nicotinic Acid (niacin, Vit B3), and Ezetimibe. Resins and Ezetimibe are used as adjuncts while the other ones are main drugs.

Q: What two major adverse effects do Statins, Fibrates, and Nicotinic Acid have in common? A: Hepatotoxicity and Rhabdomyolysis — the lysed muscle tissue can clog up kidney and cause kidney failure. Monitor the hepatotoxicity with liver function tests, and monitor for any increase in CK levels in the blood to detect rhabdomyolysis. If the patient has muscle pains, STOP THE TREATMENT!!

Q: With what class of drugs do you have to watch out for inability to absorb Vitamins A,D,E,K? A: Resins — because they remove bile salts from your system, which are needed to carry vitamin ADEK into your body.

Q: What class of drug do you need to treat with HMG CoA Reductase blockers in order to prevent the adverse effects of increased triglycerides (which is at the expense of decreased cholesterol levels that you want)? A: Resins — Cholestyramine and Colestipol

Q: What class of hyperlipoproteinemia drugs are contraindicated in patients who have hypertriglyceridemia? A: Resins — Cholestyramine and Colestipol

Q: What class of hyperlipoproteinemia drug is also used for treating obstructive jaundice because it removes bile salts from your body? A: Resins — Cholestyramine and Colestipol

Q: What class of hyperlipoproteinemia drug is contraindicated in pregnancy because it prevents the synthesis of cholesterol, and therefore prevents the synthesis of progesterone? A: Statins — Lovastatin, Simvastatin, Atorvastatin, Rosuvastatin

Q: What drugs or substances should you NOT use with statins? A: Don’t use with fibrates or niacin, because they all have the same adverse effects. Also don’t use with substances/drugs that inhibit CYP3A4 (i.e. grapefruit juice), which is needed to metabolize statins.

Q: Which statin drug has a very long half-life and therefore can be used anytime of day and also has antioxidant properties? A: Atorvastatin

Q: How do you prevent the itching and flushing adverse effects in nicotinic acid? A: give aspirin along with the drug. Aspirin blocks COX, so prostaglandin can’t be made.

Q: Which hyperlipoproteinemia drug decreases cholesterol absorption in the GI and increases LDL uptake into the cells, causing an overall lowering of LDL in the plasma? A: Ezetimibe — use as an adjunct. adverse effect is diarrhea.

Q: What anti-obesity drug releases norepinephrine as well as dopamine? A: Phendimetrazine

Q: What is the best way to increase HDL and decrease LDL, more than anything else? A: EXERCISE!!!

ANTIMICROBIALS — GENERAL PRINCIPLES

Q: What’s the difference between Prophylactic vs. Empiric vs. Therapeutic Treatment? A: Prophylaxis = give beforehand to prevent disease. Empiric = give when your patient is at risk of dying and you don’t have time to find out what it is yet. Therapeutic = give when you know what condition the patient has.

Q: Why would sub-inhibitory concentration be useful? A: Because it can enhance host immune defenses, leading to resolution, but only when the host has a strong immunity and not immunocompromised.

Q: What is the name of the effect that states that the more pathogen concentration you have, the more drug concentration you need to resolve? A: Innoculum Effect

Q: What effect do you see when the drug binds to an organelle or ribosome in the bacteria, leading to continuous killing, even after stopping the dose? A: Post-Antibiotic Effect — so must give in bolus dosing to give patient the time to recover from the toxicity. i.e. Aminoglycosides

Q: When would you use concentration-dependent drugs? A: When the drug must enter the organism, like ribosomal drugs. You must give enough so that the drug can enter the cells.

Q: When would you use time-dependent drugs? A: When the drugs target a certain time period during the cell cycle, like those targeting cell-wall synthesis. You give the drug over a long period of time to ensure that the bacteria will be exposed to the drug at a time when it is dividing.

Q: How do beta-lactam and amikacin work in synergy? A: Beta-lactams poke holes in the bacterial cell and amikacin enter and bind to the 30s ribosome to do its job.

Q: What two drugs are given together in synergy because they sequentially block the folate pathway? A: Sulfomethoxazole and Trimethoprim (SMX-TMP or Cotrimoxazole) — SMX blocks dihydropteroate Synthase and TMP blocks dihydrofolate reductase.

Q: What drug is given with penicillin drugs in synergy to block the bacteria’s drug-inactivating enzymes? A: Clavulanic Acid, Sulbactam, Tazobactam.

Q: In what kind of treatment should you limit to using only a single drug? A: Prophylaxis, because you want to prevent resistance from forming. On the contrary, yet for the same reason, you would want to give multiple drugs for therapeutic treatment to fully kill the bacteria.

Q: What prophylaxis do you give to prevent rheumatic fever in Group A Strep? A: Penicillin G

Q: What cephalosporin drugs are the drug of choice for Gram negative anaerobes (like abdominal infections or obstetrical (PID) where there is no O2? A: Cefoxitin and Cefotetan — both are second generation cephalosporins

Q: What bacterial agent would beta-lactamase inhibitors not work against? A: MRSA, because the method of resistance is due to mutated PBP, not beta-lactamases. It would also not work with any organism with ESBLs, like Gram-neg bacteria with plasmid

Q: What other cell wall inhibitors can you use for empiric therapy for crash patients? A: Monobactam (Aztreonam) and Carbapenem (Imipenem, Meropenem, Ertapenem).

Q: What is the drug of choice for animal bites? A: Augmentin

Q: What drug treats gram-negative aerobes only and is the second drug of choice for pseudomonas? A: Aztreonam, like aminoglycosides. In contrast, carbapenems are broad spectrum, and good for both gram positive and negative

Q: What drug inhibits the excretion of imipenem, making you require less dose of it, so you can prevent the adverse effects of seizures and renal failure? A: Cilastatin.

Q: What carbapenem can you use to treat UTI, but at the same time can give you renal failure? A: Imipenem

Q: What is the BEST carbapenem to use because it goes to the CNS and can use against ESBLs but there is not much supply of it somehow? A: Meropenem

Q: What drugs can also be used to fight bacteria with ESBLs like meropenem but doesn’t cross CNS like meropenem? A: Ertapenem.

Q: What drug binds D-ala-D-ala in the PBP of the bacteria, which can be mutated as their mechanism of resistance? A: Vancomycin

Q: What is the drug of choice for MRSA? A: Vancomycin

Q: What drug can be used to treat pseudomembranous colitis due to Clostridium dificile (like from Clindamycin use)? A: You could use vancomycin, BUT metronidazole is used today. We won’t start using vancomycin until the bacteria becomes resistant to metronidazole.

Q: If vancomycin fails to treat VRSA, what’s the next drug you should use? A: Linezolide

Q: If Linezolide doesn’t work, what do you use to treat staph aureus? A: Daptomycin or Tigecycline

Q: What drug can give you renal toxicity because of its renal excretion, Ototoxicity, and Red Man Syndrome? A: Vancomycin

Q: What is the condition where you get hypertension and facial flushing, after being infused with drug too quickly and too much H2 released? A: Red Man Syndrome — it is NOT an allergic reaction.

Q: What drug must be given at 7.4 pH because it doesn’t kill bacteria well in acidic environment? A: Aminoglycosides — Kanamycin, Neomycin, Streptomycin, Tobramycin, Netilmycin, Amikacin, and Gentamycin.

Q: Which drug does NOT treat anaerobic bacteria because it requires O2-dependent pumps to get into the cells? A: Aminoglycosides

Q: What drug is similar to tetracyclines and synergistic with Rifampin? A: Tigecycline

Q: What drug can treat VRE, Acinebacter, and other gram-negative bacteria but NOT pseudomonas? A: Tigecycline

Q: What drug has very similar mechanisms and adverse effects as tetracyclines, but does not have any known mechanisms of resistances yet? A: Tigecycline

Q: What drug is so lipid soluble that it needs to go through enterohepatic circulation in order to be conjugated in the liver to albumin by glucuronosyl transferase so it can become more water-soluble and extreted? A: Chloramphenicol… but this can prevent bilirubin from binding, which goes to brain, and gives you kernicterus and gray baby syndrome.

ANTIMICROBIALS — SULFONAMIDES AND QUINOLONES

Q:What drugs resemble and compete with PABA (needed for bacteria to synthesize folic acid) and inhibits Dihydropteroate Synthetase (which is only found in bacteria, not humans)? A: Sulfonamides

Q: What is the most frequently used sulfonamide? A: Sulfamethoxazole. the other two are sulfisoxazole and sulfadiazine.

Q: What drug is excreted by the kidneys but has limited solubility in the urine and therefore can crystallize in the renal tubules? A: Sulfonamides — so tell patient to drink a lot of water.

Q: What happens when drugs compete with albumin, displacing its conjugation with bilirubin, letting the unconjugated bilirubin go to the brain in the fetus or newborn? A: Kernicterus.. happens in sulfonamides, Ceftriaxome, Chloramphenicol.

Q: What drug inhibits dihydrofolate reductase (which is found in humans) from combining two dihydrofolate acids together to form tetrahydrofolate in the folate pathway? A: Trimethoprim (TMP)

Q: What drug is made of sulfa drug + TMP? A: Cotrimoxazole — it decreases resistance risks, and since it inhibits folate, it has anti-cancer effects.

Q: What drug got resisted when the bacteria increased PABA production, or decreased sensitivity of dihydropteroate synthetase to the drug? A: Sulfonamides

Q: What is the drug of choice for strep pyogenes if the patient has penicillin allergies? A: TMP, because TMP has no sulfa group.

Q: What drug can treat Nocardia, pneumocystis, toxoplasma, and conjunctivitis due to chlamydia in children, urethritis/cervicitis due to chlamydia in mothers? A: TMP

Q: What drug do you use to treat uncomplicated UTI, Topical Burn Prophylaxis, and prophylaxis for opportunistic infections in HIV patients (i.e. toxoplasma when CD4<100, PCP when CD4<200) A: TMP-Sulfa

Q: What drug do you use for Rheumatic Fever prophylaxis in strep pyogenes if the patient is allergic to penicillin? A: TMP-Sulfa

Q: What drug has anti-cancer effects and can give you pancytopenia? A: TMP

Q: What drug can increase your transaminase (ALT) levels and give you hepatotoxicity if you have HLA-B 5701 genes? A: Sulfonamides

Q: What is the mechanism of action for quinolones?
A: Inhibits DNA Gyrase, Topoisomerase 2 and 4, and therefore prevents supercoils from forming, killing the bacteria and having post-antibiotic effects.

Q: What quinolones can you use for community-acquired pneumonia?
A: Levofloxacin or Moxifloxacin.

Q: What drug causes rupture of achilles tendon (and degenerates cartilage) and therefore contraindicated in kids under 18 and in pregnancy? A: Quinolones

Q: What can quinolones do to your heart? A: Prolong QT

Q: Women taking quinolones have to watch out for what? A: Candida overgrowth

ANTIMICROBIALS — ANTI-MYCOBACTERIAL DRUGS

Q: What are two unique features of the cell wall of tuberculosis? A: high-lipid content (and therefore not killed in phagocytes), and acid fast cell wall (resistant to gram staining). “Myco” in latin means “waxy” …. Mycobacterium means “waxy bacteria.”

Q: How long does it take to treat TB and how long does it take before it gains resistance? A: takes loooong time to treat (i.e. 2 years) but it rapidly gains resistance (can gain as fast as 2 weeks)… so stick with the treatment and be patient!

Q: What gene responsible to the activation of the isoniazid prodrug does the TB delete to become resistant to isoniazid? A: Kat G Gene

Q: What gene encoding the binding site of isoniazid prodrug does the TB delete to become resistant to isoniazid? A: INH A Gene

Q: What anti-mycobacterial drugs form anti-nuclear antibodies, especially if you are a slow acylator? A: Isoniazid.

Q: What are the two major age-related adverse effects of isoniazid? A: Hepatitis, Jaundice

Q: What adverse effects are you preventing by giving Vitamin B6 with Isoniazid? A: Peripheral and Central Neuropathy. B6 is used in CSF production. Also, obviously, you are preventing vitamin B6 deficiency.

Q: What deficiency are you at risk of getting when you are taking isoniazid to treat TB? A: Vitamin B6 deficiency

Q: What is the second drug of choice for TB treatment? A: Rifampin

Q: Why don’t you use Rifampin when you’re on oral contraceptives A: Because Rifampin induces CYP450, which metabolizes oral contraceptives.

Q: What is the mechanism of action for rifampin? A: Inhibits DNA-dependent RNA polymerase in bacteria –> cidal against both intra and extracellular organisms.

Q: Besides treating Mycobacteria, rifampin is good as as prophylaxis against what organisms? A: Staph, Neisseria meningitidis, H. influenza, Enterobacteriae, and Pseudomonas… therefore good for CNS shunt surgery.

Q: Why don’t you take rifampin with isoniazid? A: Because they both have the adverse effect of hepatitis, because it is metabolized in the liver.

Q: What is the biggest adverse effect of ethambutol? A: Retrobulbar neuritis, leading to red/green color-blindness.

Q: What are the two phases of the standard regimen for TB treatment? A: Initial 2-month phase followed by a 4-month sterilizing phase.

Q: What drugs do you use during the initial 2-month phase if the patient is less symptomatic for TB? A: INH/RIF/PZA — Isoniazid, Rifampin, Pyrazinamide (“IRP”)

Q: What drugs do you add to the initial 2-month phase if the patient is more symptomatic for TB? A: INH/RIF/PZA + SM/EMB — Streptomycin and Ethambutol (“IRPSE”)

Q: What drugs do you use during the 4-month sterilizing phase? A: INH/RIF — Isoniazid and Rifampin (“IR”)… so in total for the whole standard regimen, remember “IRP or IRPSE, then IR”

Q: What drugs do you alternate every 9 months for the Alternative regimen for TB treatment? A: alternate between INH and RIF — Isoniazid and Rifampin — remember “IRIRIRIRIRIRIRI”

Q: What do you do if a patient tests positive for TB but has no evidence of symptoms, or if the patient has had recent contact with a TB patient? A: put them on an INH monotherapy for 6-9 months — preventative chemotherapy

Q: What drugs do you use to treat Leprosy (from mycobacteriae leprae)? A: Dapsone, Rifampin, Clofazime

Q: What anti-leprosy drug is very similar to sulfonamides in that it inhibits Dihydropteroate Synthase of the folic acid pathway? A: Dapsone

ANTIMICROBIALS — ANTI-VIRAL DRUGS

Q: What two drugs are neuraminidase inhibitors? A: Zanamivir and Oseltamivir

Q: What drug is a deoxyguanosine analogue that initially requires phosphorylation from the virus, but subsequent activation steps by host? A: Ganciclovir

Q: What is the biggest adverse effect of Ganciclovir? A: Neutropenia. Also thrombocytopenia and aspermatogenesis.

Q: What drug is used as a CMV prophylaxis in renal transplant patients? A: Valganciclovir, which is the oral prodrug of ganciclovir.

Q: Besides Foscarnet, what other drug can be used for resistant CMV strains? A: Cidofovir.

Q: What is the adverse effect of Cidofovir? A: Severe renal dysfunction

Q: Does Cidofovir require thymidine kinase to be activated? A: No, like Ganciclovir, it doesn’t require TK to be activated.

Q: If your patient has pharyngitis with exudates but lab tests come back negative for strep pneumo, what else could it be? A: EBV

Q: What do you use to treat EBV? A: Acyclovir, Valacyclovir, Foscarnet

ANTIMICROBIALS — ANTI-HIV DRUGS

Q: How does HIV attach to host cell? A: gp120 on virus attach to CD4 on T-cell. GP120/CD4 then binds to either CCR5 on macrophage or CXCR4 on T cells. The GP41 on the virus fuses with host T cell.

Q: Why is HIV difficult to treat? A: Because it mutates really fast. As a retrovirus, it has to constantly convert RNA to DNA then back to RNA, and this is process if imperfect, causing a high chance of mutation.

Q: What is the treatment of choice for preventing verticle transmission of HIV from mother to child? A: HAART

Q: What is the second and third treatment of choice for preventing verticle transmission of HIV? A: 2nd DOC = ZDV. 3rd DOC = NVP

Q: How do half of children with HIV die? Explain. A: autoimmune disease, because HIV hyperstimulates T cells, which release B cell growth factor and B cell transfforming factor. This causes the kid to become hypergammaglobulinemic (increased IgG levels). This IgG is not functional and causes autoimmune antibody disease.

Q: Which HIV drug class works by competing with RNA to bind to the reverse transcriptase, causing chain termination, but does NOT require phosphorylation for its activation? A: NNRTI (vs. NRTI, which works the same way but is a prodrug that requires phosphorylation by the host,, except Tenofovir)

Q: What drug class inhibits its own metabolism by inhibiting CYP3A4, which also metabolizes it? A: Protease Inhibitors.

Q: Zidovudine (ZDV) is also known as what? A: Azidothymidine (AZT)

Q: What drugs are the first-line NRTI for treatment of HIV in pregnancy or pediatrics? A: Zidovudine, Lamivudine

Q: What PI can boost serum levels of other PIs at low doses because it inhibits P450, which metabolizes the PIs? A: Ritonavir, and therefore it is given with almost all other PIs (Lopinavir, Fosamprenavir, Darunavir, Atazanavir)

Q: Which PI tastes bad? A: Ritonavir

Q: Which two PIs has sulfur and therefore causes Steven-Johnson Syndrome? A: Fosamprenavir and Darunavir (DRV)

Q: What antifungal drug interferes with ergosterol synthesis by inhibiting squalene epoxidase, leading to toxic accumulation of squalene in the keratin? A: Terbinafine (compare this with azoles, which also interferes with ergosterol synthesis but by inhibiting 14-alpha-demethylase)

Q: What treats ring worm (superficial mycosis)? A: Terbinafine

Q: What are the two interesting adverse effects of terbinafine? A: Taste disturbance, Steven Johnson Syndrome

Q: What drug like amphotericin B also binds ergosterol, and is also a polyene? A: Nystatin

Q: What can Gentian Violet treat? A: Candida… but it makes your skin purple and a lot of folks don’t like that.

ANTIMICROBIALS — ANTI-MALARIAL DRUGS

Q: Which malarias are found in blood only? A: P. falciparum and P. malariae — therefore you must treat with systemic drug.

Q: Which malarias are found in liver as well as blood? A: P. vivax and P. ovale (vivax and ovale both have the letter V. Liver has the letter V.) — therefore you must treat with both systemic and a liver drug

Q: What is prophylaxis against chloroquine-resistant malaria? A: Mefloquine

Q: A traveler came back to the U.S and developed chills + fever that showed a cyclic pattern of every 72 hrs… what is it? A: P. malariae!! It is a systemic malaria so you treat it with a systemic drug, like Chloroquine or Quinine

Q: A traveler came back to the U.S and developed chills + fever that showed a cyclic pattern of every 48 hrs… what is it? A: P. vivax or ovale!! It is a liver malaria so you treat with systemic + liver drugs (primaquine)

Q: Mefloquine, the prophylaxis for chloroquine-resistant malaria, should not be given to who? A: Mental patients.. because the drug causes neuropsychiatric symptoms… you don’t want to worsen them. Also don’t give to pregnant women during first trimester… can lead to stillbirths.

Q: How did malaria gain resistance to chloroquine? A: By increasing efflux pump, decreasing the drug’s entrance into the organism.

Q: Why is the combo pyrimethamine+sulfodoxine no longer used? A: Because it causes Steven-Johnson Syndrome and Toxic Epidermal Necrolysis.

Q: What is the drug of choice for Malaria? A: Chloroquine

Q: What if chloroquine doesn’t work, like in those strains of P. vivax in New Guinea and Indonesia? A: Treat with Hydroxychloroquine (don’t get confused with mefloquin, which is used for chloroquine-resistant malaria PROPHYLAXIS).

Q: What antimalarial drug works by increasing toxic levels of reactive oxygen species and H2O2 (like nifurtimox in antiparasitic drugs)? A: Primaquine, which is the malarial liver drug. Because it increases reactive oxygen, it is contraindicated in G6PD deficient patients, who also have an increased reactive oxygen level in their blood system, causing hemolysis.

Q: What does a patient have when they took a parasitic treatment and developed pneumonia, fever, and eosinophilia? A: Loeffler’s Syndrome — shows that the work has already penetrated the blood and has become invasive, and that the drug you gave didn’t work.

Q: What is the mechanism of action of niclosamides? A: inhibits parasite mitochondrial phosphorylation

Q: What is the drug of choice for Leishmania? A: Stibogluconate dosium

Q: What is the mechanism of action for Stibogluconate dosium? A: It is an antimony analogue that inhibits glycolysis and fatty acid metabolism, starving the parasite.

Q: How does Pyrantel Pamoate work? A: They depolarize the neuromuscular junction, causint a persistent activation of nicotinic receptors, leading to paralysis of the worm. The pinworms, roundworms, and hookworms detach from your intestinal wall and you poop it out.

Q: What drug causes host cell to produce superoxide and H2O2, leading to peroxidation of the parasite? A: Nifurtimox